Myofascial Pain Syndrome in the Craniomandibular Region

Myofascial Pain Syndrome in the Craniomandibular Region#

Jan Dommerholt, PT, MPS*

Craniomandibular disorders (CMD) are characterized become chronic pain patients (3-5). Patients with by a combination of symptoms that may include pain, persistent craniomandibular pain without objective tenderness and dysfunction of the temporomandibular clinical or radiographic findings are especially joint, the mouth and the occlusal contacts, the cervical challenging not only to the general dentist, but also to spine, and the muscles of mastication. Patients may orthodontists, oral surgeons, TMJ specialists, and other present with local dentoalveolar pain; muscle pain; clinicians. Some patients may be considered good head, facial and neck pain; sounds during condylar candidates for splint therapy. Others are referred to movements; deviations and limitations of mandibular oral surgeons when common dental procedures fail to movements; altered occlusal relations; parafunctions offer relief. Some frustrated pain patients may even and poor oral habits; and functional limitations of request surgical treatment in an effort to eliminate mastication. Craniofacial pain conditions have special chronic craniomandibular pain (6). emotional and psychological meaning. The face, the It is generally accepted that CMD have a mouth, speech, and other oral functions are essential for multifactorial etiology (7). Although many diseases, nearly all human interactions; craniofacial pain such as dental disease, infections and tumors, can be conditions interfere with such functions and with the associated with pain, most chronic pain problems are ability to communicate. thought to be musculoskeletal in nature. Different Approximately 10% of the general population perspectives of the primary source of pain have passed experience craniomandibular pain (1). The prevalence the revue. Some researchers and clinicians have is estimated to range from 0% to 10% for males and emphasized joint dysfunction (8, 9); others have from 2% to 18% for females. The prevalence in focused more on muscular problems (10-12). The children and adolescents is estimated to range between relation between occlusion and CMD has been the 2% to 6% (2). Pain complaints range from acute and subject of several investigations (13-16). Multiple transient conditions such as toothaches to chronic studies have considered the impact of stress on CMD ailments, such as trigeminal neuralgia and and in particular the impact of stress on pain and temporomandibular disorders. While in the majority of tenderness of the masticatory muscles (17-19). With pain patients, pain decreases over time with or without the advancement of the pain sciences, more and more treatment, for a small percentage the pain complaint emphasis is placed on peripheral and central nervous persists. Similarly to other musculoskeletal pain system sensitization (20-23). problems, between 5% and 15% of all CMD patients

# Previously published as Dommerholt, J: “El sindrome de dolor miofasical en la region craneomandibular”. In: Padrós Serrat, E. (ed) Bases diagnosticas, terapeuticas y posturales del functionalismo craniofacial. Madrid, Ripano, 2006: 564-581 * Bethesda Physiocare / Myopain Seminars, 7830 Old Georgetown Road, Suite C-15, Bethesda, MD 20814 – 2440, USA; +301.656.5613 (phone); +301.654.0333 (fax); [email protected]

Functional relations with spine dysfunction defined concept of “myofascial pain syndrome” (MPS) need to be considered in the management of patients described by Simons, Travell and Simons (33). MPS is with craniomandibular pain syndromes (24, 25). the main subject of this chapter and can be described as Rocabado has developed a pragmatic approach the sensory, motor, and autonomic symptoms caused by incorporating the intricate relationships between the myofascial trigger points. A myofascial trigger point cervical spine and mandible and temporomandibular (MTrP) is clinically defined as a hyperirritable spot in function. He has demonstrated that centric position can skeletal muscle that is associated with a hypersensitive only be achieved when there is a balance between the palpable nodule in a taut band. The spot is painful on position and movement patterns of the subcranial compression and can give rise to characteristic referred region, the mid and lower cervical spine, the hyoid, and pain, referred tenderness, motor dysfunction, and the mandible (26, 27). A detailed biomechanical autonomic phenomena (33). Although there are many assessment is important. Rocabado’s “pain map” is an peer-reviewed studies and reports in the international excellent tool to determine which joint structures cause medical literature supporting the importance of MTrPs or may contribute to the pain complaint (see in clinical practice, many of these reports are not Rocabado’s chapter in this book for a more detailed included in major medical library indices. Fortunately, description of his approach). several prominent researchers are now investigating In addition to a biomechanical joint MTrPs and the results of many of these studies support assessment, clinicians need to include a detailed the theoretical foundations and clinical applications. evaluation of the muscles in the cervical and Nevertheless, there is a substantial lack of basic craniomandibular region. Numerous studies of scientific studies; in general, MTrPs are underexplored craniomandibular muscle pain and dysfunction have by research investigators (34). incorporated the “research diagnostic criteria for A better understanding and working temporomandibular disorders” by Dworkin and knowledge of MTrPs and MPS will provide dentists, LeResche, which include a section on muscle orthodontists, oral surgeons, and other clinicians with dysfunction (28). The research criteria were developed an effective approach to relieve human suffering, and to classify and quantify both the physical and contribute significantly to their patients’ quality of life. psychosocial components of temporomandibular If MTrPs are not considered in the differential dysfunction. Although the criteria are widely used in diagnosis, a common cause of patients’ pain complaints dental research, they are remarkable simplistic where it will be overlooked (34, 35). MPS should be considered involves muscle dysfunction. The section “Axis I, with any pain syndrome in the head, neck, face, and Group I, Muscle Disorders” of the criteria includes only TMJ area (12, 33, 36). Dentists need to be aware that two options to describe muscle dysfunction: tender apparent dental or TMJ pain does not necessarily have muscles with or without limited mouth opening. a dental or joint origin (37). The inclusion of the word “diagnostic” in the Myofascial pain tends to be dull, poorly title of Dworkin and LeResche’s classification criteria localized, and deep, in contrast to the precise location may be interpreted that the criteria can be used in of dental pain and cutaneous pain. Muscles can refer clinical practice. However, research criteria do not pain to other deep somatic structures, such as fascia, necessarily provide a mechanism for clinical diagnosis. joints, viscera, and other muscles (38). Clinically, For example, MTrPs, myositis, and other less common referred pain is confusing to many clinicians, as conditions affecting muscles, such as myoadenylate frequently, patients complain more of pain in the deaminase deficiency or fascioliasis can not be referred pain zone and not necessarily of pain in the diagnosed using the research criteria. Therefore, immediate area of a MTrP. Signs and symptoms Dworkin and LeResche’s criteria do not provide any suggestive of non-odontogenic pain include an starting points to treat patients with craniomandibular inadequate local dental cause for the pain; a recurrence muscular dysfunction in clinical settings, even though of pain in spite of reasonable dental therapy of the tooth they have been validated for research purposes (29-32). or TMJ; poor lasting pain relief after local anesthetic blocking; positive findings with Rocabado’s pain map; Myofascial Pain Syndrome postural abnormalities such as forward head posture; In the dental literature, muscle pain with or and other pain problems, such as chronic and recurrent without limits in mouth opening is commonly referred headaches and widespread chronic pain conditions. to as “myofascial pain dysfunction syndrome,” a Patients with MPS usually have a history of somewhat unfortunate term, as it is often confused and acute or chronic muscle overload. In dental practice, used interchangeably with the more practical and better MPS is commonly seen in patients with a history of

2 bruxism or clenching (12, 39-41). A common The second edition summarizes significant progress in iatrogenic cause of MPS occurs when patients are the understanding of the pathophysiological basis of the required to keep their mouths open for prolonged clinical presentations associated with MTrPs. The periods of time during dental procedures (42). Patients manuals have been translated into six different with MPS in the head-neck region often are unable to languages, including Spanish. Several other MTrP relax their muscles in between contractions, i.e., the manuals have been published in Switzerland, the masseter, sternocleidomastoid and trapezius muscles. United States and the UK (46, 55, 56). The muscles are in continuous contracture, which can Several assessment and treatment approaches result in muscle ischemia, fatigue and pain (23, 43, 44). have emerged independently of each other both in Europe and in the United States, including myofascial Historical Overview of Myofascial Pain Syndrome trigger point therapy (USA), neuromuscular technique MTrPs are the principal characteristic of MPS. or NMT (UK), neuromuscular therapy, also abbreviated During the past nearly 200 years, numerous authors as NMT (USA), and manual trigger point therapy have described MTrPs in the English, German, Dutch, (Switzerland). It is not a coincidence that these and French medical literature, illustrating that approaches share many similarities and have common musculoskeletal pain due to MTrPs is very common goals and objectives (57). Recent insights in the nature, (45, 46). Already in 1816, British physician Balfour etiology and neurophysiology of MTrPs and their described MTrPs as “nodular tumours and thickenings associated symptoms have propelled the interest in the which were painful to the touch, and from which pains diagnosis and treatment of persons with MPS shot to neighbouring parts.” Balfour speculated that the worldwide (58). nodules were due to inflammation of the fibrous connective tissue in muscle (47). Historically, multiple Diagnostic Criteria terms have been used to describe muscle pain A diagnosis of MPS can be made only by syndromes, many of which would have been diagnosed palpation. There are no laboratory tests, imaging as MPS using the current definition, including studies, or standardized diagnostic criteria to make an fibrositis, myofasciitis, muscular rheumatism, initial diagnosis of MPS. While this may suggest, that rheumatic myositis, muscle hardening, myogelosis, a diagnosis of MPS can not be established, clinical myalgia, myofascial pain, and even fibromyalgia (45). evidence combined with multiple scientific studies and In 1938, British rheumatologist Kellgren case reports support the practice of evaluating patients published a seminal paper describing specific referred for the presence of MTrPs. In a survey of physician pain patterns of many muscles and spinal ligaments members of the American Pain Society, 85% of 493 following injections of hypertonic saline. In 1952, medical pain specialists, representing fourteen medical Travell wrote the first of many articles introducing the specialties, agreed that MPS is a distinct syndrome myofascial genesis of pain illustrated by specific (59). MPS may actually be the most overlooked referred pain patterns of over 30 muscles (48). Travell diagnosis in chronic pain patients (60). The diagnosis (1901 - 1997) has been referred to as the pioneer in the depends on the clinician’s skills, training and treatment of musculoskeletal pain through the experience in taking a patient’s history, performing a recognition of MTrPs. She coined the term comprehensive examination, and assessing patients for “myofascial pain syndrome” to describe pain as a result MTrPs. Clinicians should not assume knowing how to of trigger points in muscle, tendon, skin, fascia, and identify MTrPs without specific training (61, 62). ligaments (the term “trigger point” was introduced by Unfortunately, few medical, dental and allied health Steindler in 1940 (49)). Several of Travell’s school curricula include education and training in the subsequent papers included referred pain patterns assessment and treatment of MTrPs. Most clinicians relevant for head, neck, facial, and craniomandibular trained in the diagnosis and treatment of MTrPs have pain (50-52). Travell and Simons authored the classic been trained through post-graduate continuing two-volume text “Myofascial Pain and Dysfunction - education programs, such as the Interessengemeinschaft The Trigger Point Manual.” The first volume was f!r Myofasziale Triggerpunkttherapie (Society for published in 1983 for the upper half of the body Myofascial Trigger Point Therapy) in Switzerland followed by the second volume in 1992 for the lower (www.imtt.ch) and the Janet G. Travell, MD Seminar half (53, 54). The second edition of the first volume, Seriessm in the US (www.painpoints.com). The authored by Simons, Travell and Simons, was released International Myopain Society has established a in 1999 and includes contributions by experts in the multidisciplinary international committee to design a growing field of myofascial pain and dysfunction (33). study model for validation of diagnostic criteria. The

3 committee aims to establish reliable methods for diagnosis of MPS, determine the interrater reliability of MTrP examination, and determine the sensitivity and specificity with which classification criteria can distinguish patients with MPS from healthy control subjects (63). Simons, Travell and Simons defined a MTrP as a localized spot of tenderness in a nodule of a palpable taut band of contractured muscle fibers (33). Taut bands are examined by gently palpating a muscle perpendicular to the direction of the muscle fibers. Taut bands need to be differentiated from more generalized muscle spasms, that can be defined as Figure 1 – c. Intra-oral palpation of the masseter muscle electromyographic activity as a result of increased neuromuscular tone of the entire muscle (64, 65). A taut band feels like a rope or string of contractured fibers, that may extend from one end of the muscle to the other end. There are two basic palpation techniques for the proper identification of MTrPs. A flat palpation technique is used for example with palpation of the temporalis and masseter muscles (Figure 1). A pincher palpation technique is used for example with palpation of the sternocleidomastoid and the upper trapezius muscles (Figure 2).

Figure 2 – a. Pincher palpation of the sternocleidomastoid muscle

Figure 1 – a. Flat palpation of the temporalis muscle

Figure 2 – b. Pincher palpation of the trapezius muscle

Two recent studies have established excellent overall interrater reliability of the clinical examination used to establish the presence of MTrPs (62, 66). To make a diagnosis of MPS, the minimum essential features that need to be present are a taut band, an Figure 1 – b Flat palpation of the masseter muscle exquisitely tender spot or nodule in the taut band, and

4 the patient’s recognition of the pain complaint with specifically mention MTrPs, they described many of pressure on the tender nodule (62). Simons, Travell the symptoms commonly associated with MTrPs, such and Simons add a painful limit to stretch range of as increased myofascial tenderness, hardness, referred motion as the fourth essential criterion (33). Taut pain causing headaches, and central sensitization as a bands and MTrPs are found in asymptomatic result of persistent nociceptive input from pericranial individuals and are only considered clinically relevant and extracranial muscles (76). Many case reports when the patient recognizes the elicited pain or when describe that MTrPs can cause or contribute to the functional limitations imposed by the taut band persistent headaches, facial pain, and contribute to mechanical dysfunction secondary to temporomandibular pain (50, 77-80). Carlson muscle shortening (61, 67). The presence of a local demonstrated the clinical significance of referred pain twitch response, referred pain, and the by eliminating pain of the masseter muscle by treating electromyographic demonstration of endplate noise MTrPs in the trapezius muscle (81). increase the certainty and specificity of the diagnosis. Many scientific studies and review articles have focused on muscle referred pain (12, 23, 44, 82- Local Twitch Response 93). Referred pain is not specific to MTrPs, but it is A local twitch response (LTR) is elicited by more common and much easier to elicit over MTrPs either strong digital palpation or needling/injection of a than over other structures (85). Hong found that all taut band or MTrP, that results in an involuntary brief subjects reported referred pain with pressure directly burst of motor action potentials propagated only by over active MTrPs, but less than 50% of subjects fibers of that taut band or by fibers of a taut band from reported referred pain with pressure over latent MTrPs another muscle (68-70). A LTR is a spinal cord reflex, (85). Compared to active MTrPs, latent MTrPs do not mediated through the spinal cord without supraspinal produce spontaneous pain; they require more pressure influences (69). During the physical examination, a to elicit localized and referred pain (33). Normal LTR confirms the presence of a MTrP. Although the muscle tissue and other body tissues, including skin, LTR can occur during physical examination of MTrPs, zygopophyseal joints, and internal organs may also eliciting a LTR is not essential for making a diagnosis refer pain to distant regions with prolonged and of MPS. Eliciting a LTR manually or with needling sufficient mechanical pressure (67, 89, 94-99). In the can be difficult and rather painful for patients, which orofacial region, it is relevant that the teeth can also suggests that a LTR perhaps originates from refer pain to other areas, including the TMJ and the stimulation of sensitized nociceptors in the MTrP sinuses (75). region rather than exclusively from mechanical By mechanically stimulating an active MTrP, stimulation (38). Eliciting a LTR during needling patients often report the development of referred pain in procedures is critical for the successful treatment of a fairly consistent patterns, either immediately or after a MTrP (61, 71). Close proximity to the MTrP is brief 10-15 second delay. Mechanical stimulation may essential (68). Gerwin and Duranleau were able to consist of manual pressure, needling of the MTrP, objectively visualize the LTR using diagnostic movement of the involved body region, or even sonography, following stimulation of a MTrP by prolonged postural strains, such as forward head insertion of a hypodermic needle (72). High resolution posture or prolonged mouth opening. Usually, pain in sonography was however, not sensitive enough to reference zones is described as deep tissue pain of a visualize the actual MTrP (73). dull and aching nature. However, some patients report burning or tingling sensations or other paresthesia (89, Referred Pain 100). In that sense, the term “referred sensation” Since Kellgren’s early studies on referred pain reflects the clinical condition sometimes more from muscle, multiple clinical reports have been accurately than the established term “referred pain.” published on referred pain from MTrPs (74). Referred Common referred pain patterns for nearly all skeletal pain is challenging for clinicians, as the patient’s muscles are documented by Travell and Simons (33, perception of localization of pain can be very different 53, 54). Dejung and colleagues have modified several from the original source of pain (75). To better referred pain patterns in their recent publication on appreciate the clinical implications of referred pain MTrPs (55). from MTrPs, a more extended review is included in this chapter. Although Asina and colleagues did not

Neurobiology of Referred Pain of the interleukins IL-1#, IL-6 and IL-8. Especially IL- In recent years, much new information has 8 can cause hyperalgesia that is independent from become available about the neurobiology of muscle prostaglandin mechanisms. Via a positive feedback referred pain (23, 38). Although the majority of data loop, IL-1 beta can also induce the further release of has been obtained from animal experiments, it is bradykinin (114). Bradykinin triggers the release of probably applicable to patients. Mense and colleagues calcitonin gene related peptide (CGRP), which reduces have demonstrated that skeletal muscles have different the effectiveness of acetylcholinesterase (115-117). types of nociceptors (101-103). Under normal The combination of endogenous substances reinforces conditions, skeletal muscle nociceptors require high the observed hyperalgesia. Injections of bradykinin and intensities of nociceptive stimulation involving high- serotonin into the temporal muscle of healthy threshold mechanosensitive neurons, that do not volunteers caused more severe pain than either respond to moderate local pressure, contractions or bradykinin or serotonin by itself (118). Following muscle stretches (65). Muscle nociceptors are activated muscle trauma multiple substances are released by endogenous pain-producing substances such as simultaneously, which appears to occur in MTrPs as bradykinin or serotonin. At least one of the muscle well. In their studies of the neurochemical milieu of nociceptors is specifically sensitive to ischemic MTrPs, Shah and colleagues at the U.S. National conditions (104). Institute of Health have confirmed increased Local ischemia is associated with MTrPs. concentrations of bradykinin, substance P, TNF-", Looking at MTrPs from a biomechanical perspective, it interleukins, CGRP, and norepinephrine in active is conceivable that at the cytoskeletal level, myosin MTrPs when compared with latent MTrPs and healthy filaments literally get stuck in the Z band of the control subjects (119). In addition, the pH of the MTrP sarcomere. During sarcomere contractions, titin site was significantly lower in the active MTrP group. filaments are folded into a gel-like structure at the Z The endogenous substances bind to specific band. In MTrPs, gel-like titin appears to prevent the receptor molecules in the membrane of nociceptive myosin filaments from detaching. The myosin nerve endings, including the so-called purinergic and filaments may actually damage the regular motor vanilloid (VR-1) receptors. Purinergic receptors bind assembly and prevent the sarcomere from restoring its adenosine triphosphate and stimulate nociceptors resting length (105). The contracted sarcomeres are accordingly. VR-1 receptors are especially sensitive thought to reduce the local circulation by compressing under conditions of lowered tissue pH and muscle the capillary blood supply and thus cause a significant ischemia. Mense suggested that pain during tooth lack of local oxygen. One study has shown that the clenching, bruxism, and tension-type headaches is oxygen saturation in the center of a MTrP is less than mediated by the VR-1 receptor molecule (44). 5% of normal (106). Histological studies also suggest Bradykinin, serotonin and prostaglandin interact at that MTrPs are ischemic: ragged-red and moth-eaten many levels at the vanilloid receptors (120). fibers have been identified in myogeloses and MTrPs Referred pain is generated by central (107-110). Moth-eaten fibers indicate a change in the mechanisms dependent on peripheral input from the distribution of mitochondria or the sarcotubular system, referred pain area. MTrPs are a source of ongoing while ragged-red fibers reflect an accumulation of peripheral nociceptive input. Long-term nociceptive mitochondria (111). Both are usually associated with input into the spinal cord or brain stem causes changes muscle ischemia, denervation, or strenuous exercise in function and connectivity of sensory dorsal horn (112). Simons suggested that myogeloses and MTrPs neurons or neurons in the trigeminal nucleus caudalis may represent the same phenomenon (113). respectively (21, 44, 121, 122). The ongoing afferent Local hypoxia is associated with the release barrage into the dorsal horn and the trigeminal nucleus of endogenous inflammatory substances, such as results in central sensitization, the unmasking of prostaglandin, bradykinin, serotonin, capsaicin, sleeping receptors in the dorsal horn, referred pain, and histamine, and interleukins. Activation and hyperexcitability (121, 123-125). There is considerable sensitization of muscle nociceptors leads to evidence that both neurokinin and N-methyl-D- inflammatory hyperalgesia, an activation of high aspartate (NMDA) receptors are involved in triggering threshold nociceptors associated with C fibers, and an hyperalgesia and the MTrP-induced hyperexcitability increased production of bradykinin. Furthermore, of dorsal horn cells and brainstem nociceptive neurons bradykinin stimulates the release of tumor necrosis (21, 44, 126). factor (TNF-"), which in turn activates the production

In MTrPs, low-threshold mechanosensitive neurons may also get activated (127). Strong or long- lasting nociceptive input from damaged muscle tissue or from MTrPs results in spatial summation in the dorsal horn or brain stem and the appearance of new receptive fields, which means that input from previously ineffective regions can now stimulate the neurons. In other words, the population of dorsal horn sensory neurons responding to the MTrP afferent input grows larger. As interneurons are located over various segments, the expansion may reach sensory neurons that supply peripheral areas outside the initial MTrP area. The expansion of pain areas is commonly seen in patients with headaches, whiplash, and other diagnoses (128, 129). There is no nociceptor activity in the referred pain area (44). Masseter MTrPs can trigger maxillary and mandibular tooth pain, TMJ pain, facial pain, including Figure 3 – b. Referred pain pattern of the superficial pain commonly associated with sinusitis, deep ear pain, masseter muscle tinnitus, and frontal and temporal headaches (Figure 3).

Temporalis MTrPs can induce maxillary tooth pain and temporal headaches (Figure 4).

Figure 3 – a. Referred pain pattern of the deep masseter muscle

Figure 4 – Referred pain pattern of the temporalis muscle

Medial pterygoid MTrPs result in pain in the mouth, tongue, pharynx, hard palate, and behind the temporomandibular joint (Figure 5).

Figure 5 – Referred pain pattern of the medial Figure 7 – Referred pain pattern of the digastric muscle pterygoid muscle

Lateral pterygoid MTrPs cause TMJ pain and pain in MTrPs in the platysma muscle cause referred pain the maxillary sinus (Figure 6). sensations over the lateral surface of the mandible. Most cervical muscle MTrPs have referred pain patterns into the head and face regions (Figure 8) (33). Simons, Travell and Simons described the formation of so-called satellite MTrPs in referred pain areas (33).

Figure 6 – Referred pain pattern of the lateral pterygoid muscle

MTrPs in the posterior belly of the digastric muscle refer pain to the upper part of the sternocleidomastoid muscle, the front of the throat, and sometimes into the occiput. MTrPs in the anterior belly of the digastric muscle refer pain to the mandibular incisors, the alveolar ridge, and the tongue (Figure 7). Figure 8 – a. Referred pain pattern of the sternocleidomastoid muscle, sternal portion

Electromyographic Findings Hubbard and Berkhoff recorded both low- amplitude continuous action potentials (10-50 microvolts), which they labeled “spontaneous electrical activity,” and intermittent spikes (100-600 microvolts) from active MTrPs (130). The electrical activity was only present in sites of active MTrPs and was absent in adjacent non-tender muscle tissue. Subsequent studies indicated that the low-amplitude noise-like potentials represented grossly abnormal endplate activity (EPN) as compared to the normal miniature endplate potentials (MEPP) commonly reported by electromyographers (131-134). In the EMG literature, abnormal EPN is assumed to be associated with normal motor endplates and normal disease-free muscles (135). However, the physiology literature indicates that EPN represents an abnormal Figure 8 – b. Referred pain pattern of the concentration of acetylcholine up to three times normal sternocleidomastoid muscle, clavicular portion levels (132, 134, 136, 137). Recent studies by Shah and colleagues confirmed high concentrations of acetylcholine at MTrP sites (119, 138). EPN is not exclusive to MTrPs. Already in 1956, Liley reported that a normal endplate could exhibit abnormal noise-like discharge patterns by mechanically stressing the endplate (139). Simons suggested that Liley’s observation may help to account for the activation of MTrPs by mechanical overload or mechanical trauma (34). In 1997, Maselli confirmed that damage to the endplate caused by the tip of the advancing EMG needle could convert normal miniature endplate potentials (MEPP) to EPN, because of a massive release of acetylcholine (140). Brown and Varkey suggested that the spikes, that Hubbard and Berkhof had observed in MTrPs, could also arise from mechanical stimulation of the endplate, however, Wiederholt had already provided evidence that the spikes indeed originated in the neuromuscular junction (130, 135, 141). In Maselli’s words, the origin of the spikes “corresponds to single muscle fiber action potentials postsynaptically activated by suprathreshold end-plate noise” (140). By using a very slow insertional technique as described by Simons and Figure 8 – c. Referred pain pattern of the trapezius colleagues, EPN from MTrP can be reliably observed muscle (132, 134).

Integrated Trigger Point Hypothesis significant decrease in heart rate, and systolic and Combining all available supporting evidence diastolic blood pressure, indicating a significant of the existence of MTrPs, Simons has recently increase in parasympathetic activity (151). proposed a new “integrated trigger point hypothesis” The integrated trigger point hypothesis is (33). The integrated trigger point hypothesis has summarized in figure 9. The hypothesis is a “work in evolved through several steps of progress since its first progress” that is beginning to be subjected to rigorous introduction as the “energy crisis hypothesis” in 1981 scientific review and verification. (142). The hypothesis builds on the finding that excessive amounts of acetylcholine from the motor nerve terminal cause miniature motor endplates potentials that produce the endplate noise observed with needle EMG of MTrPs. The excessive acetylcholine maintains a sustained depolarization of the postjunctional membrane, which in turn results in an excessive release of calcium from the sarcoplasmic reticulum and sustained sarcomeric contractions. Shenoi and Nagler suggested that an impaired re-uptake of calcium into the sarcoplasmic reticulum induced by calcium channel blockers may cause MTrPs (143). According to the integrated trigger point hypothesis, the sarcomeric contractions cause local hypoxia, reducing the available energy supply. The combined decreased energy supply and increased metabolic demand possibly may explain the common finding of abnormal mitochondria in the nerve terminal, referred to as “ragged red fibers” (Henriksson et al. 1993; Henriksson 1999). The local energy crisis would also impair the calcium pump, which would provide another mechanism of the sustained contractures. The calcium pump is responsible for returning intracellular calcium into the sarcoplasmic reticulum against a concentration gradient, which requires a functional energy supply. Figure 9 – Integrated trigger point hypothesis As reviewed, hypoxia also stimulates the release of endogenous substances, resulting in hyperalgesia, central sensitization, and stimulation of It is likely that new studies will demonstrate that there the autonomic nervous system, which has been shown are many other factors to consider. For example, to increase endplate potentials. For example, an preliminary data from current studies by Shah and increase in psychological arousal resulted in an colleagues provide already new insights in the basic immediate increase of endplate spike rates (144, 145). pathophysiology of MTrPs (119). The finding of Autogenic relaxation and the administration of the increased levels of several endogenous substances in sympathetic blocking agents phentolamine and the neurochemical milieu of MTrPs, including phenoxybenzamine inhibited the autonomic activation bradykinin, serotonin, prostaglandin, and CGRP, (146-148). Induced autonomic nerve activity would combined with the finding of a lowered pH may alter explain autonomic phenomena commonly seen with the current understanding of motor endplate MPS, and further contribute to the abnormal release of dysfunction in relation to MTrPs. Both CGRP and a acetylcholine, possibly by increasing the permeability lowered pH can effectively reduce the function of of calcium channels in the cell membrane of the nerve acetylcholinesterase, which could cause an overall terminal (149, 150). A recent study examined the increase of available acetylcholine (115-117). At the effects of MTrP massage therapy on the cardiac same time, a lowered pH can activate peripheral autonomic tone in healthy subjects. The researchers nociceptors and trigger capsaicin- sensitive afferents, observed that following MTrP therapy, there was a which in turn can release several of the endogenous 10

substances from their peripheral endings, including A sudden onset or a clear remembrance of the CGRP (152-154). A pH of 6.1 resulted in a threefold onset of pain may indicate an acute activation of MTrPs increase of the basal CGRP release, which was entirely due to mechanical stress, but it may also indicate a dependent on the presence of extracellular calcium sudden change in the patient’s environment or habits. (155). Bradykinin caused a 50% increase of the basal The mechanical stress may be the result of sudden or CGRP release which was also dependent on the abrupt movements, motor vehicle accidents, falls, presence of extra-cellular calcium (155). Endogenous fractures, joint sprains or dislocations, a direct blow to substances such as bradykinin, serotonin and a muscle, joint, or mandible, excessive exercise or prostaglandin, clearly interact at multiple levels, activity, or performing new or unusual activities. A including at the vanilloid receptors (120). Although slow insidious onset is usually the result of chronic the relevance of these interactions has not been studied overloading of tissue, such as habitual chewing gum or specifically in relationship to MTrPs, it is likely that tobacco, postural imbalances, poor body mechanics, future studies will reveal new aspects of their repetitive movements, and tension as a consequence of pathophysiology. Interestingly, Shah and colleagues psychological or emotional stress (57). established an immediate drop in the concentrations of Clinicians should consider both the sensory several substances with dry needling of a MTrP (119). and mechanical aspects of MTrPs. The physical If the integrated trigger point hypothesis is basically examination must include a thorough evaluation of correct, MTrPs are primarily a muscle disease with MTrPs relevant to the patient’s current pain secondary but important sensory, motor and autonomic presentation. The patient’s current area(s) of pain can phenomena (156). be visualized through patient pain drawings. While patients communicate their pain patterns, the clinician Clinical Applications can begin identifying those muscles and active MTrPs MPS and MTrPs should be considered in the most likely involved in the pain problem. For example, differential diagnosis of craniomandibular pain and in a patient with complaints of temporal headaches, the temporomandibular joint dysfunction, migraines, pain complaint may direct the clinician to the tension headaches, radiculopathies, complex regional sternocleidomastoid, trapezius, temporalis and inferior pain syndrome, whiplash injuries, and most other pain oblique capitis muscles. The patient’s head posture in syndromes. To diagnose and manage MPS, clinicians slight side bending and rotation may implicate the must become well-trained in the identification of scalene muscles, although the referred pain pattern MTrPs. Through inactivation of MTrPs, clinicians can from MTrPs in the scalene muscles does not include the facilitate return to function and elimination of pain in head region. If the patient in addition presents with a both acute and chronic pain patients. Together with the paradoxical breathing pattern, it will be necessary to patient, ultimate functional goals need to be discussed. examine and treat the accessory breathing muscles as For some patients, eating solid foods may be the final well, including the pectoralis minor, scalenes, goal. For others, it may be restoring sleep, regaining sternocleidomastoid and upper trapezius musculature sexual activity, or returning to work. Treating MTrPs that may be overloaded due to increased demands. is merely an effective tool to assist patients in regaining Teaching the patient a normal diaphragmatic breathing lost function (157). There are many different manual pattern and fostering awareness of relaxation techniques, including myofascial release techniques, techniques for the upper chest and neck region will aid compression, trigger point compression combined with in the long term management of the headaches. active contractions of the involved muscle, muscle Dentists should limit their direct treatment to muscles energy or post-isometric relaxation, connective tissue cranially from the clavicles to stay within the scope of stretches, and general massage therapy. Needling dental practice. techniques include superficial and deep dry needling, Habitual postural patterns need to be assessed and trigger point injections (61, 158). For persistent (162-164). Does the patient have a forward head cases, botulinum toxin can be used as it blocks the posture? Are there certain work postures or habits that release of acetylcholine (159, 160). Throughout the maintain the head in an antero-position? Forward head treatment process, patients must be educated regarding posture is associated with multiple static and dynamic the etiology, perpetuating factors, and self- changes in total body alignment. Patients with forward management. Patients must learn to modify their head posture present with posterior cervical rotation of behaviors and avoid overloading the muscles without the upper cervical and subcranial motion segments, a resorting to total inactivity (161). posteriorly displaced mandible, altered occlusion, as

well as shoulder girdle protraction, internally rotated When using injection needles, the use of a humeri, increased thoracic kyphosis, a loss of lumbar local anesthetic is more comfortable for many patients lordosis, and an increase in posterior pelvic rotation. and results in a longer lasting reduction in MTrP pain Dentists need to be familiar with the consequences of (167). The use of solid acupuncture needles versus forward head posture. For example, if a patient with injection needles has not been examined at this time. forward head posture receives a splint, the dentist may After identifying and manually stabilizing the tender have to adjust the splint after the patient’s head posture area in the taut band with the fingers, the needle is has been corrected by a physical therapist. Close quickly passed through the skin and then into the working relationships between dentists and physical trigger zone. A LTR or a report of referred pain therapists are very important and benefit patients. indicates that the trigger zone has been entered. A small Simons, Travell and Simons advocated the amount, usually 0.1 or 0.2 ml, of local anesthetic may spray and stretch technique, which combines use of a be injected into the trigger zone. There is no benefit to vapocoolant spray with passive stretching of the muscle adding steroids. The needle is withdrawn to just below (33). Application of vapocoolant spray stimulates the skin, the angle of the needle changed, and the thermal and tactile A-beta skin receptors, thereby needle is again passed through the muscle to another inhibiting C-fiber and A-delta fiber afferent nociceptive trigger zone. A conical volume of muscle can thus be pathways and muscle spasms, MTrPs, and pain when examined for active trigger points without withdrawing stretching. Prior to applying the spray and stretch the needle through the skin. The trigger zone is method, the patient is positioned comfortably. The explored in this manner until no further LTRs are muscle involved is sprayed with a few sweeps of a obtained. Dry needling a MTrP is most effective, when vapocoolant spray, after which the muscle is stretched LTRs are elicited (71, 138). A LTR has been shown to passively. With the muscle in the stretched position, the inhibit abnormal endplate noise. Current (unpublished) spray is applied again over the skin overlying the entire research strongly suggests that a LTR is essential in muscle, starting at the trigger zone and proceeding in altering the neurochemical milieu of a MTrP (Shah, the direction of and including the referred pain zone. 2003, personal communication). Patients commonly Following the stretch and spray, the area is heated with describe an immediate reduction or elimination of the a moist heat pack for 5-10 minutes. The patient is pain complaint after eliciting LTRs. Once the pain is encouraged to move the body part several times reduced, patients can start active stretching and through the full range of motion. The spray and stretch strengthening programs. Eliciting a LTR with dry technique can be used in physical therapy as a separate needling is usually a rather painful procedure. Post- modality or following myofascial trigger point needling soreness may last for one to two days, but can injections. Muscle stretching can be combined with easily be distinguished from the original pain muscle energy techniques or post isometric relaxation, complaint. At this point, the taut band is usually gone, during which the muscle is stretched after a brief sub- and the spontaneous pain of the trigger point has maximal isometric contraction. All techniques are used subsided. Patients who have previously undergone diagnostically and therapeutically (61, 158). Some treatment can tell when MTrPs remain, and when they patients can learn to use spray and stretch techniques at have been sufficiently inactivated. A knowledgeable home. Self treatment programs can be very effective patient will urge the clinician to continue in an area (165). until a key MTrP is inactivated, at which time there will Inactivation of MTrPs by injection or dry be a noticeable decrease in pain. The process is needling appears to be the result of the mechanical repeated until the symptomatic MTrPs are treated action of the needle, since it can be successfully throughout the functional muscle unit (61). accomplished without the use of local anesthetics or There is no limit to the number of MTrP that other materials. In 1979, Lewit confirmed that the can be needled. Common sense and patient comfort effects of needling were primarily due to mechanical dictate restraint. Nevertheless, when treating a regional stimulation of a MTrP with the needle. Dry needling of MPS, a sufficient number of muscles in the region must a MTrP using an acupuncture needle caused immediate be treated to resolve the problem and allow effective analgesia in nearly 87% of needle sites. In over 31% of post-needling stretching. All the muscles in a functional cases, the analgesia was permanent. Twenty percent muscle unit must be released and returned to full had several months of pain relief, 22% several weeks, length, if possible, either by needling or by MTrP and 11% several days. Fourteen percent had no relief compression and stretching. Inadequate treatment that at all (166). leaves critical MTrPs within a functional muscle unit

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